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Homozygous deletions of the p15 (MTS2) and p16 (CDKN2/MTS1) genes in adult
T-cell leukemia
Y Hatta, T Hirama, CW Miller, Y Yamada, M Tomonaga and HP Koeffler
Department of Medicine, UCLA School of Medicine, Cedars-Sinai Research
Institute, CA 90048, USA.
Adult T-cell leukemia (ATL) is associated with prior infection with human
T-cell leukemia virus type I (HTLV-I). Twenty to 40 years often elapse from
viral infection to overt ATL, suggesting that other genetic events must
occur to produce frank leukemia. The p15 (MTS2) and p16 (CDKN2/MTS1) genes
located on chromosome 9p have been implicated as candidate tumor-suppressor
genes in several types of tumors. We examined for alterations of these
genes in ATL using Southern blot and polymerase chain
reaction-single-strand conformation polymorphism analyses. Both p15 and p16
genes were homozygously deleted in 4 of 23 acute/lymphomatous ATL (17%). An
additional 3 (13%) and 4 (17%) acute/lymphomatous samples had hemizygous
deletions in at least one exon of p15 and p16, respectively. One of 14
chronic ATL samples had a homozygously deleted p16 gene and another had a
hemizygous deletion of p16. Neither homozygous nor hemizygous deletions of
the p15 gene were found in chronic ATL. In total, 10 of 37 (27%) ATL
samples had loss of the p15 and/or p16 genes. No point mutations of the p15
and p16 genes were found. The ATL patient with a homozygously deleted p16
in the chronic phase rapidly progressed to acute ATL and died within 6
months of the initial diagnosis. One instructive patient had no detectable
deletion of the p15 and p16 genes during the chronic phase of ATL but had a
homozygous deletions of both genes when she progressed to acute ATL. Our
results suggest an association of p15/p16 deletions with development of
acute ATL.
Volume 85,
Issue 10,
pp. 2699-2704,
05/15/1995
Copyright © 1995 by The American Society of Hematology
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